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Moos RH, Solomon GF. Minnesota multiphasic personality inventory response patterns in patients with rheumatoid arthritis. J Psychosom Res. 1964;8:17-28

George Freeman Solomon was born on 25^th November 1931 in Freeport, State of New York (he died on 7^th October 2001 in Los Angeles, California). Stimulated by his father Joseph, a child psychiatrist, Solomon dedicated his entire life to “psychoimmunology”. He was a founding member of the PsychoNeuroImmunology Research Society and its fourth president in 1997-1998 (www.pnirs.org).

His partner was Rudolf Hugo Moos, a professor of psychiatry born in 1934 in Berlin and still professor emeritus in Stanford University Medical Center. The grandfather of Moos – also named Rudolf Moos – was the founder of the still-existing German shoe company Salamander in 1903. The Jewish family of Moos was forced to immigrate to the U.K. in 1939 and later to the USA.

In their common work, Solomon and Moos linked personality and disease, which they studied in patients with rheumatoid arthritis (RA) in 1964 (1, 4-6). For these studies, they used the Minnesota Multiphasic Personality Inventory (MMPI). They carried out their work in the Stanford University School of Medicine, Palo Alto, California. In 1964, they wrote:

“The rheumatoid arthritic patients scored significantly higher on scales reflecting (1) physical symptoms; (2) depression, apathy and lack of motivation; (3) general “neurotic” symptoms; (4) psychological rigidity and (5) similarity to other psychosomatic conditions. The arthritics appeared to be more neurotic, depressed, anxious, masochistic, and over-controlled than their healthy family members.”

They cited older work from the late 1940s of D. Cohen (3) and D. Wiener (4) who similarly studied patient with arthritis with comparable results, but due to unclear disease classifications in Cohen’s and Wiener’s early publications, the work of Solomon and Moos was much stricter and focused on definite RA. They followed established criteria of the American Rheumatism Association, later called American College of Rheumatology (ACR). Direct comparisons of women with RA and their unaffected healthy sisters (4, 5) complemented these studies.

Furthermore, Solomon & Moos correctly recognized that the responses of RA patients may be due to “actual limitations [editor: by the inflammatory disease], to the effects of hospitalization, or to a changed physical-social reality, and may, therefore, not reflect pathological personality dynamics” (1). In other words, the results are not dependent on a “rheumatic personality” but are a consequence of the chronic inflammatory disease. This was very far-sighted because most other psychoanalytically driven investigators at the time were propelled by the idea of an a priori existing personality that stimulated a given disease.

Today, we well know that chronic inflammatory diseases can have a strong influence on the brain, which most obviously can be seen as chronic fatigue, anxiety, and major depression (7). The concept of a “rheumatic personality” did not stand the test of time but the highly relevant influence of inflammation on brain function in patients with RA – suggested by Solomon and Moos – did. Furthermore, preceding trauma in childhood and adolescence was clearly associated with a higher risk of RA (8). The latter findings link Solomon’s psychoimmunology to the direct stimulation of RA (summarized in a recent book, 9).

The journal Neuroimmunomodulation published several papers on the link between damaged brain and RA (10-15).

References

1. Moos RH, Solomon GF. Minnesota multiphasic personality inventory response patterns in patients with rheumatoid arthritis. J Psychosom Res. 1964;8:17-28
2. Cohen D. Psychological concomitants of chronic illness: A study of emotional correlates of pulmonary tuberculosis, peptic ulcer, the arthritides, and cardiac disease. Doctoral dissertation, University of Pittsburgh (1949).
3. Wiener DN. Personality characteristics of selected disability groups. J Clin Psychol. 1948;4:285-90
4. Moos RH, Solomon GF. Psychologic comparisons between women with rheumatoid arthritis and their nonarthritic sisters. I. Personality test and interview rating data. Psychosom Med. 1965;27:135-149
5. Moos RH, Solomon GF. Psychologic comparisons between women with rheumatoid arthritis and their nonarthritic sisters. II. Content analysis of interviews. Psychosom Med. 1965;27:150-164
6. Solomon GF, Moos RH. The relationship of personality to the presence of rheumatoid factor in asymptomatic relatives of patients with rheumatoid arthritis. Psychosom Med. 1965;27:350-360
7. Fatigue in Rheumatic Arthritis. Issue Supplement to Rheumatology. https://academic.oup.com/rheumatology/issue/58/Supplement_5
8. Dube SR, Fairweather D, Pearson WS, Felitti VJ, Anda RF, Croft JB. Cumulative childhood stress and autoimmune diseases in adults. Psychosom Med. 2009;71:243-250
9. Straub RH. Early trauma as the origin of chronic inflammation. Springer, Heidelberg, 2023
10. Philipp J, Baerwald CG, Seifert O. Association between the Ile164 β2 Adrenergic Receptor Polymorphism and Fatigue in Patients with Rheumatoid Arthritis. Neuroimmunomodulation. 2023;30:93-101
11. Straub RH, Detert J, Dziurla R, Fietze I, Loeschmann PA, Burmester GR, Buttgereit F. Inflammation Is an Important Covariate for the Crosstalk of Sleep and the HPA Axis in Rheumatoid Arthritis. Neuroimmunomodulation. 2017;24:11-20
12. Petersen LE, Grassi-Oliveira R, Siara T, dos Santos SG, Ilha M, de Nardi T, Keisermann M, Bauer ME. Premature immunosenescence is associated with memory dysfunction in rheumatoid arthritis. Neuroimmunomodulation. 2015;22:130-137
13. Silverman MN, Sternberg EM. Neuroendocrine-immune interactions in rheumatoid arthritis: mechanisms of glucocorticoid resistance. Neuroimmunomodulation. 2008;15:19-28
14. Lorton D, Lubahn CL, Estus C, Millar BA, Carter JL, Wood CA, Bellinger DL. Bidirectional communication between the brain and the immune system: implications for physiological sleep and disorders with disrupted sleep. Neuroimmunomodulation. 2006;13:357-374
15. Cutolo M, Straub RH. Stress as a risk factor in the pathogenesis of rheumatoid arthritis. Neuroimmunomodulation. 2006;13:277-282